Radioimmunoassay of atrial natriuretic factor: Human plasma levels
Abstract
A simple and sensitive radioimmunoassay procedure has been developed for the determination of atrial natriuretic factor (ANF) in human plasma. The rabbit antiserum was obtained from a commercial source. ANF was extracted from plasma using an octadecasilyl silica cartridge with a recovery of 78.7%. HPLC of the plasma extract showed the presence of one immunoreactive peak of ANF correponding to its low molecular weight form. Plasma ANF in humans increased from 8.0 ± 2.2 in upright position to 20.0 ± 5.9 fmol/ml (n = 6) in downward position (p < 0.005).
References (11)
- R. Palluk et al.
Life Sci
(1985) - P.R. Salacinski et al.
Anal. Biochem
(1981) - K. Nakao et al.
Biochem. Biophys. Res. Commun
(1984) - I. Tanaka et al.
Biochem. Biophys. Res. Commun
(1984) - J. Gutkowska et al.
Biochem. Biophys. Res. Commum
(1984)
Cited by (114)
Recombinant bovine growth hormone-induced reduction of atrial natriuretic peptide is associated with improved left ventricular contractility and reverse remodeling in cardiomyopathic UM-X7.1 hamsters with congestive heart failure
2007, Growth Hormone and IGF ResearchTo assess the effect of short-term treatment with GH on left ventricular contractility and remodeling, after the development of heart failure in cardiomyopathic hamsters (CMH).
Two groups of 200-day-old UM-X7.1 CMH received daily subcutaneous injections of recombinant bovine (rb) GH (1 mg/kg/day) or 0.9% NaCl for 40 days. Golden Syrian hamsters (GSH) were used as controls. At 240-day-old, the hamsters were randomly subjected to (i) assessment of left ventricular systolic function in a Langendorff perfused mode followed by the determination of the passive diastolic pressure–volume relationship and morphometric measurements; (ii) assessment of left ventricular mRNA expression of genes belonging to the fetal gene program including atrial (ANP) and brain (BNP) natriuretic peptides and cardiac myosin heavy chain isoforms and of the circulating levels of the natriuretic peptides.
Hearts from CMH were hypertrophied and dilated (p < 0.05) compared to hearts from GSH, along with a ∼10-fold increase in the circulating ANP and BNP levels. Left ventricular BNP and ANP mRNAs were elevated by 2- and 3-fold, respectively, compared to GSH. rbGH reduced both ANP mRNA and ANP circulating levels by 34% (p < 0.01) but did not significantly modulate BNP levels. This effect was associated with a preserved systolic function and reverse remodeling as assessed by a leftward shift of the passive diastolic pressure–volume relationship indicating reduced ventricular dilatation.
The data show that a short-term administration of GH in the terminal phase of the disease confers cardioprotection by attenuating systolic dysfunction and by inducing beneficial reverse remodeling.
Pattern of sodium handling and its consequences in patients with preascitic cirrhosis
1995, GastroenterologyThe initial abnormalities in the renal sodium handling in patients with cirrhosis before developing ascites remain unknown. The aim of this study is to further characterize sodium metabolism and the effects of sodium loading in preascitic cirrhosis. Eight male, preascitic patients with cirrhosis and 6 volunteers had their daily urinary sodium excretion level measured while on a strictly metabolically controlled diet, first consisting of 20 mmol then of 200 mmol sodium per day each for 7 days. Central blood volume, plasma norepinephrine, and atrial natriuretic factor levels were measured during each diet. Preascitic patients with cirrhosis had significantly less daily urinary sodium excretion on both diets. Volume expansion in the patients with cirrhosis was indicated by significantly greater weight gain and higher atrial natriuretic factor levels for each diet. Patients with cirrhosis had central blood volume expansion (1725 ± 54 mL/m2) compared with controls (1495 ± 81 mL/m2; P = 0.03) on a low-sodium diet. This increased significantly in the controls (1864 ± 164 mL/m2; P = 0.04) on a high-sodium diet, associated with suppression of plasma norepinephrine, but not in the patients with cirrhosis (1679 ± 107 mL/m2; P > 0.05). Failure of further central blood volume expansion in the patients with cirrhosis on high-sodium diet in the presence of significant weight gain suggests maldistribution away from the effective arterial blood volume. This study provides further reasons why preascitic patients with cirrhosis might benefit from sodium restriction.
The aim of this study was to assess baroreceptor function in well-compensated cirrhosis by determining the forearm vascular, renal, and humoral responses to sustained baroreceptor deactivation. The effect of sodium status on baroreceptor function was also assessed. Eight cirrhotic patients and 10 age- and sex-matched controls were studied twice after a 20 mmol and 200 mmol of sodium/d diet for 7 days. Systemic and renal hemodynamics, renal sodium handling, forearm blood flow, and neurohurioral factors were assessed before, during, and after the application of lower body negative pressure (LBNP) for 1 hour. Controls and cirrhotic patients had similar baseline mean arterial pressure, heart rate, forearm and renal hemodynamics. High-sodium intake resulted in suppression of sympathetic nervous activity in the controls (plasma norepinephrine, 1.06 ± 0.11 mmol/L on low vs. 0.76 ± 0.08 nmol/L on high sodium; P = 0.01) but not in the cirrhotic patients (1.35 ± 0.22 mmol/L on low vs. 1.26 ± 0.11 mmol/L on high sodium; P > 0.05). Both groups responded to LBNP with significant further increases in plasma norepinephrine, resulting in significant decreases in forearm blood flow on both sodium diets. Controls also responded with a significant worsening of renal hemodynamics on low-sodium diet only, but this was not observed in the cirrhotic patients on either diet. Therefore, in well-compensated cirrhotic patients: (1) sympathetic activation occurs despite an adequate, effective arterial filling, and this may contribute to sodium retention; and (2) baroreceptor function is normal. Apparent end organ unresponsiveness within the renal circulation may account for the lack of renal hemodynamic changes to reflex sympathetic stimulation.
Plasma atrial natriuretic peptide during spontaneous bronchoconstriction in asthmatics
1995, PeptidesThe aim of this work was to establish the role of endogenous ANP during a spontaneous asthma attack. Forced expiratory lung volume in 1 s (FEV1), cardiovascular parameters, and plasma ANP, cAMP, and cGMP were measured for 60 min before and 10 min after treatment with a bronchodilator in 10 asthmatics. The results show that in the presence of moderate bronchoconstriction, FEV1 was 54 ± 3% (±SE); ANP levels initially were slightly elevated at 47 ± 10 pg/ml and decreased to 26 ± 3 pg/ml (p < 0.05) over 60 min, with no change in FEV1. Following salbutamol inhalation, FEV1 increased to 77 ± 4% with no change in ANP. We conclude that endogenous ANP does not act as a bronchodilator in asthmatics with moderate bronchospasm.
Negative chronotropic effect of the atrial natriuretic peptide in an anaesthetized dog model
1994, European Journal of PharmacologyThe effects of atrial natriuretic peptide (ANP) on heart rate and on the chronotropic response induced by angiotensin II were evaluated. The action of angiotensin II, injected into the sinus node artery, on heart rate was determined in anaesthetized and vagotomized dogs pretreated with β-adrenoceptor antagonist (n = 9), before and after the infusion of physiological and pharmacological doses (10 and 50 ng/kg per min) of ANP. ANP plasma concentrations were determined by radioimmunoassay. Compared to the baseline concentration values (117±3 pg/ml), a slight increase was produced by the lower dose (293±45 pg/ml), whereas a significant augmentation was noted with the higher dose of ANP (1024±255 pg/ml). The basal heart rate and mean systemic arterial pressure were decreased (26.3 and 13.5%) during the intravenous infusion of the physiological dose of the peptide and were significantly reduced (32.5 and 29.2%, P < 0.05) by the administration of the pharmacological dose of ANP. Angiotensin II had a positive chronotropic effect (29 ± 3 beats/min) that was significantly inhibited by the pharmacological dose of ANP. Our results suggest that ANP might have a role in the control of heart rate.
Clinical Relationships of Cyclic GMP
1994, Advances in PharmacologyThe purpose of this chapter is to review current knowledge on the clinical use of cyclic guanosine monophosphate (cGMP) measurements as markers of endogenous and exogenous ANP effects. cGMP production through the stimulation of particulate guanylate cyclase is induced by the action of atrial natriuretic peptide (ANP) on target cells. In humans, the use of radioimmunoassay has enabled the determination of plasma and urinary cGMP levels along with the development of a potential tool to detect and follow physiological and pharmacological changes evoked by ANP. The reviewed data addressed in this chapter shows that plasma and urinary levels of cGMP are correlated with plasma ANP levels within a wide range from physiological to pharmacological concentrations. cGMP measurement in plasma and urine can therefore be seen as a potentially useful tool to monitor the effects of exogenous ANP and the results of physiological maneuvers where blood volume and atrial stretch are expected to change.